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Kidney oxygenation during water diuresis and endothelial function in patients with type 2 diabetes and subjects at risk to develop diabetes.

The aim of the present study was to examine the relationship among water diuresis-induced changes in renal oxygenation, endothelial function, and various metabolic parameters in type 2 diabetic patients and healthy subjects at risk of type 2 diabetes. Thirty-eight subjects with type 2 diabetes (D: age, 54 +/- 10 years, mean +/- SD, 24 men) and 7 healthy subjects with parental history of type 2 diabetes or with impaired glucose tolerance (IGT) (relatives [R]: age 46 +/- 11 years, 4 men) were included. Laser Doppler imaging scanning was used to measure vasodilatation in the forearm skin in response to iontophoresis of 1% acetylcholine (Ach) and 1% sodium nitroprusside (SNP), and ultrasound was used to measure the flow-mediated dilation (FMD) and nitroglycerin-induced dilation (NID) in the brachial artery. Renal oxygenation was assessed by magnetic resonance imaging (MRI) before and during water diuresis. A decrease in the magnetic parameter R2* implies an increase in oxygenation. Renal medullary oxygenation did not improve with diuresis in either group (D: -0.5 +/- 1.9, R: -0.4 +/- 2.1, P = not significant [NS]). The renal cortical oxygenation showed a small, but statistically significant, improvement after diuresis in the 2 groups (D: -0.6 +/- 1.1, R: -0.5 +/- 0.5, P <.05). There were no correlations between the change in cortical R2* (R2* post-minus R2* prewater diuresis) and the micro- and macrovascular reactivity. The postdiuresis renal cortical R2* was negatively correlated with both the Ach- and SNP-induced skin vasodilation (% change over baseline)(r = -.40, P <.01 and r = -.39, P <.05, respectively), while no correlation existed with the FMD and NID. The baseline renal cortical oxygenation was also negatively correlated with the SNP-induced skin vasodilation (r = -.36, P <.05) and positively correlated with the fasting plasma glucose, total cholesterol, and vascular cell adhesion molecule (VCAM) concentrations (r =.34, P <.05, r =.31, P <.05 and r =.37, P <.05, respectively). These preliminary findings suggest an association between the kidney cortical oxygenation and the skin microvascular reactivity, glycemia, and lipidemia. Water diuresis failed to produce an improvement in renal medullary oxygenation in both patients with diabetes and subjects at risk for diabetes.

Aged↗

Contralateral response in renal pelvic pressure and diuresis during increasing ipsilateral pelvic pressure and flow: a study of the normal and denervated upper urinary tract in pigs.

OBJECTIVE: To examine, in young pigs, changes in baseline pelvic pressure and diuresis in the contralateral kidney during conditions of increasing pelvic pressure and perfusion with isotonic saline in the ipsilateral renal pelvis; the role of a reno-renal nervous mechanism was examined by denervating the kidneys, and the effect of bladder filling on these variables assessed. MATERIALS AND METHODS: Female pigs (37-40 kg) were assessed under general anaesthesia. Transparenchymally, one 6 F and two 6 F catheters were introduced into the right and left renal pelvis, respectively. Through a bladder incision an 8 F catheter was introduced 10 cm into the right ureter to collect urine and the orifice closed around the catheter. For bladder drainage and to measure bladder pressure a 10 F catheter was placed in the bladder and both the 8 F and 10 F catheters lead out through the urethra. In group A, five animals served as controls, with group B comprising eight with intact nerves and group C eight with denervated kidneys. In group B and C the left renal pelvis was perfused with isotonic saline at 2, 4, 6, 8, 10, 12 and 16 mL/min while the bilateral pelvic pressure and right renal diuresis were recorded; the bladder was kept empty and 0.5 h later the left pelvis was perfused with 10 mL/min while the bladder catheter was closed. Perfusion continued until micturition occurred. The bilateral pelvic pressure, bladder pressure and right renal diuresis were recorded. In group C the kidneys were surgically denervated, dividing all adhesions and all connective tissue around the pelvis and the vascular pedicle. The renal artery was freed to the aortic level. RESULTS: During the pressure-perfusion study the mean (sd) right pelvic pressure was 7.4 (0.2) mmHg in group B and 8.6 (0.2) mmHg in group C. The diuresis from the right kidney in both groups was similar and the same as that in group A. The perfusion rate and pressure on the left side had no influence on pelvic pressure and diuresis on the right side. During perfusion with a full bladder the right pelvic pressure was 8.6 mmHg in group B and 9.5 mmHg in group C. Diuresis in group B was approximately 0.6 mL/min and a little higher in group C, at approximately 1 mL/min, but identical to that in group A. CONCLUSION: These results indicate that a reno-renal reflex mechanism has no apparent role in young pigs during pressure-perfusion measurements with an empty or full bladder.

Animals↗

Postnatal diuresis and respiratory distress syndrome in infants receiving mechanical ventilation.

Measurements of body water homeostasis and pulmonary function were obtained in 24 infants with respiratory distress syndrome requiring mechanical ventilation during the first five days of life to determine the relationship of diuresis to improvement in pulmonary function. Initial diuresis (output intake ratio greater than 0.8) occurred at 24 hours, maximum diuresis (output intake ratio greater than or equal to 1.6) at 40 hours, and initial improvement in pulmonary function (fall in AaDO2 greater than 50 mm Hg) at 48 hours. Urine flow rates over four-, eight-, or 12-hour periods were quite variable and correlated poorly with improvement in pulmonary function. Reduction in body weight was a more accurate indicator of total changes in body water than urine output, output intake ratio, or fractional excretion of sodium. Although there was a temporal relationship of loss of body water and improvement in pulmonary function by analysis of means, no cause-and-effect relationship could be found on a case-by-case analysis. Five of 24 infants demonstrated improvement in pulmonary function prior to diuresis or reduction in body weight. Nine infants had a diuresis more than 24 hours prior to pulmonary improvement, and two infants had a diuresis without pulmonary improvement during the five-day study period. These data indicate that factors other than body water are associated with improvement in pulmonary function in infants with respiratory distress syndrome.

Age Factors↗

[Effect of dexamethasone and spironolactone therapy on diuresis and creatine clearance in premature infants with a birth weight below 1,500 g].

BACKGROUND: The aim of the study was to examine the influence of dexamethasone and spironolactone on diuresis and creatinine clearance in 8-40 day old premature infants with a birth weight less than 1500 g. PATIENTS: 85 preterm infants were included in this study. Median birth weight was 1195 g (range 560-1495), mean gestational age was 28 (range 25-34) weeks. 31 infants were given dexamethasone if bronchopulmonary dysplasia was diagnosed and 32 infants received spironolactone. Indication for spironolactone was persistent ductus arteriosus or bronchopulmonary dysplasia. METHOD: The multivariate variance analysis (MANOVA) was performed to investigate the influence of spironolactone and dexamethasone on diuresis and creatinine clearance. Additional influence of gestational age, postnatal age and fluid intake wa eliminated by the multivariate variance analysis. RESULTS: Spironolactone therapy resulted in no differences for diuresis and creatinine clearance. Dexamethasone therapy increased creatinine clearance (p < 0.05) and diuresis (p < 0.005). CONCLUSIONS: Spironolactone is not very effective in the therapy of persistent ductus arteriosus and bronchopulmonary dysplasia. Diuresis and creatinine clearance are not increased. In conclusion spironolactone is more effective in clinical conditions associated with high circulating levels of aldosterone. Dexamethasone, on the other hand, has a high effect on diuresis and creatinine clearance. The pathomechanism for the increase of parameters studied is not completely understood.

Birth Weight↗

Effect of diuresis on extracorporeal shockwave lithotripsy treatment of ureteric calculi.

OBJECTIVE: To evaluate the effect of diuresis during extracorporeal shockwave lithotripsy (ESWL) treatment of ureteric calculi. The purpose is to improve stone fragmentation and clearance rates. MATERIALS AND METHODS: One hundred and six consecutive patients with ureteric calculi at different levels were treated by ESWL using Siemens Lithostar 2 machine. Patients have been randomized into two treatment groups. The first group was treated by standard ESWL and included 54 patients. The second group was treated by ESWL with diuresis during the ESWL session. Shock waves were given at a rate of 90 shocks/minute with energy starting from 10 up to 18 KV. During the ESWL session the patient belonging to the second group received i.v. infusion of 500 ml normal saline containing 40 mg furosemide as a diuretic. The stone fragmentation and clearance rates were the two end points for evaluation. RESULTS: The average number of sessions per stone was 1.92 and 1.5 and the average number of shocks per stone was 6295 and 5300 for the first and second treatment groups respectively. Stone fragmentation rate was 47/54 (87%) and 50/52 (96.2%) and the stone clearance (success) rate was 47/54 (87%) and 48/52 (92.3%) for the first and the second groups respectively. Analysis of the results in relation to stone location showed that the two treatment groups were comparable for upper and middle ureteric calculi. However for distal ureteric stones, the addition of diuresis during ESWL was associated with a lower mean number of ESWL sessions and shocks per stone compared with standard ESWL: 1.38 and 4950 for ESWL with diuresis compared with 2.9 and 8544 for standard ESWL respectively. The stone fragmentation and 3-month clearance (success) rates were clearly higher: 93.8% and 87.5% respectively for ESWL with diuresis compared with 70.6% (for both fragmentation and clearance) with standard ESWL. CONCLUSIONS: Diuresis is a useful, inexpensive and safe adjunct to ESWL of ureteric stones. It markedly improves the results of ESWL treatment of distal ureteric stones compared with standard ESWL.

Adolescent↗

Influence of water-diuresis or saline volume expansion on deep nephron tubuloglomerular feedback.

We have recently demonstrated the existence of a tubuloglomerular feedback mechanism in juxtamedullary nephrons in rat kidneys during antidiuresis. In the present experiments, we have investigated the influence of water-diuresis on Munich Wistar rats and in homozygote Brattleboro rats. We have also observed the effect of saline volume expansion on the tubuloglomerular feedback of juxtamedullary nephrons in Munich Wistar rats. For comparison, the feedback mechanism was also studied in surface nephrons during water-diuresis in Munich Wistar rats. Measurements of flow rate in the descending limb of Henle and single nephron glomerular filtration rate (GFR) using micropuncture at the renal papilla were performed, while the ascending limb was microperfused at varying perfusion rates with a modified Ringer solution. In surface nephrons early proximal flow rate, single nephron GFR and stop-flow pressure was measured during microperfusion of the end-proximal loop. No significant changes were measured in surface nephrons during water-diuresis: the tubular flow rates, feedback responses, stop-flow pressure and stop-flow pressure changes were similar to those during anti-diuresis. In juxtamedullary nephrons, Henle loop flow rate increases during water-diuresis but the feedback-mediated flow and single nephron GFR response curves obtained during microperfusion were unaltered compared to controls. Together, these results indicate that the feedback could be more activated during water-diuresis than during control conditions. On the other hand, during saline volume expansion, reduced tubuloglomerular feedback sensitivity was found as shown earlier for surface nephrons. The reduction of tubuloglomerular feedback sensitivity therefore seems to be important in maintaining salt-, but not water-balance.

Animals↗

The effects of peripherally administered monoaminergic drugs on ethanol diuresis in rats.

The effect of peripherally administered drugs that modify monoaminergic function, on ethanol (2.0 g kg-1, intragastrically)-induced changes in urine output has been examined in rats. The alpha-noradrenoceptor agonist, clonidine (0.05-0.15 mg kg-1) produced marked urine output and potentiated slightly the diuretic effect of ethanol. The alpha-noradrenoceptor antagonist, phentolamine (1-5 mg kg-1) dose-dependently decreased ethanol-induced diuresis. p-Chloroamphetamine (0.8-2.0 mg kg-1) produced significant diuresis and potentiated the diuresis produced by ethanol. Methysergide (1.25, 2.5 mg kg-1), a 5-hydroxytryptamine receptor antagonist, had no effect on urine output while it depressed the ethanol-induced increase in urine output. Apomorphine (0.8, 1.5 mg kg-1), a dopamine receptor agonist, did not modify urine output in either control or ethanol-treated animals, while the dopamine receptor antagonist, pimozide (0.75-3.0 mg kg-1), dose-dependently decreased ethanol-induced diuresis, but had no effect on urine output in control animals. Since our previous research indicates that the intraventricular administration of drugs that alter dopaminergic and 5-HT function does not alter ethanol-induced diuresis, the interaction of these types of agents with ethanol-induced diuresis in the present study suggests that the interaction was mediated peripherally.

Animals↗

Mechanisms for the diuresis of acute cold exposure: role for vasopressin?

The hypothesis that inhibition of vasopressin (VP) secretion initiates cold-induced diuresis was tested in six Brattleboro homozygous (diabetes insipidus, DI) rats exposed to 60 min at 5 degrees C. For 9-14 days before cold exposure (CE) the rats were treated with VP (750 pg.kg-1.min-1) subcutaneously via osmotic minipumps. Eight vehicle-treated Long-Evans (LE) rats characterized the response to acute exposure at 5 degrees C. Additional groups of six to eight LE and six DI rats were infused with VP (30-90 pg.kg-1.min-1 iv) on the day of CE. The DI rats receiving chronic VP replacement and untreated LE rats exhibited cold-induced diuresis, with peak increases in urine flow (V) of 63 +/- 12 (DIs) and 29 +/- 4 (LEs) microliters.min-1 x 100 g body wt-1. LE rats acutely infused with VP exhibited a diuresis at the two lower doses (peak V was 18 +/- 3 at the 30 and 18 +/- 4 microliters.min-1 x 100 g body wt-1 at the 60 pg.kg-1.min-1 dose), but the diuretic response was completely blunted at the uppermost dose of VP. Cold-induced diuresis was absent at the lowest VP dose in the acutely infused DI rats. A pressor response (30-36 mmHg) to CE was noted with all treatment groups, including those that did not exhibit a diuresis. No changes in glomerular filtration rate (GFR) with CE were observed. These data suggest that when plasma VP levels are controlled by prolonged infusion of VP in the DI rats, other mechanisms can operate to initiate cold-induced diuresis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Urea may regulate urea transporter protein abundance during osmotic diuresis.

Rats with diabetes mellitus have an increase in UT-A1 urea transporter protein abundance and absolute urea excretion, but the relative amount (percentage) of urea in total urinary solute is actually decreased due to the marked glucosuria. Urea-specific signaling pathways have been identified in mIMCD3 cells and renal medulla, suggesting the possibility that changes in the percentage or concentration of urea could be a factor that regulates UT-A1 abundance. In this study, we tested the hypothesis that an increase in a urinary solute other than urea would increase UT-A1 abundance, similar to diabetes mellitus, whereas an increase in urine urea would not. In both inner medullary base and tip, UT-A1 protein abundance increased during NaCl- or glucose-induced osmotic diuresis but not during urea-induced osmotic diuresis. Next, rats undergoing NaCl or glucose diuresis were given supplemental urea to increase the percentage of urine urea to control values. UT-A1 abundance did not increase in these urea-supplemented rats compared with control rats. Additionally, both UT-A2 and UT-B protein abundances in the outer medulla increased during urea-induced osmotic diuresis but not in NaCl or glucose diuresis. We conclude that during osmotic diuresis, UT-A1 abundance increases when the percentage of urea in total urinary solute is low and UT-A2 and UT-B abundances increase when the urea concentration in the medullary interstitium is high. These findings suggest that a reduction in urine or interstitial urea results in an increase in UT-A1 protein abundance in an attempt to restore inner medullary interstitial urea and preserve urine-concentrating ability.

Animals↗

Genetic AVP deficiency abolishes cold-induced diuresis but does not attenuate cold-induced hypertension.

Chronic cold exposure causes hypertension and diuresis. The aim of this study was to determine whether vasopressin (AVP) plays a role in cold-induced hypertension and diuresis. Two groups of Long-Evans (LE) and two groups of homozygous AVP-deficient Brattleboro (VD) rats were used. Blood pressure (BP) was not different among the four groups during a 2-wk control period at room temperature (25 degrees C, warm). After the control period, one LE group and one VD group were exposed to cold (5 degrees C); the remaining groups were kept at room temperature. BP and body weight were measured weekly during exposure to cold. Food intake, water intake, urine output, and urine osmolality were measured during weeks 1, 3, and 5 of cold exposure. At the end of week 5, all animals were killed and blood was collected for measurement of plasma AVP. Kidneys were removed for measurement of renal medulla V2 receptor mRNA and aquaporin-2 (AQP-2) protein expression. BP of LE and VD rats increased significantly by week 2 of cold exposure and reached a high level by week 5. BP elevations developed at approximately the same rate and to the same degree in LE and VD rats. AVP deficiency significantly increased urine output and solute-free water clearance and decreased urine osmolality. Chronic cold exposure increased urine output and solute-free water clearance and decreased urine osmolality in LE rats, indicating that cold exposure caused diuresis in LE rats. Cold exposure failed to affect these parameters in VD rats, suggesting that the AVP system is responsible for cold-induced diuresis. Cold exposure did not alter plasma AVP in LE rats. Renal medulla V2 receptor mRNA and AQP-2 protein expression levels were decreased significantly in the cold-exposed LE rats, suggesting that cold exposure inhibited renal V2 receptors and AVP-inducible AQP-2 water channels. We conclude that 1) AVP may not be involved in the pathogenesis of cold-induced hypertension, 2) the AVP system plays a critical role in cold-induced diuresis, and 3) cold-induced diuresis is due to suppression of renal V2 receptors and the associated AQP-2 water channels, rather than inhibition of AVP release.

Angiotensin II↗

Role of atrial peptide in the natriuresis and diuresis that follows relief of obstruction in rat.

The present studies demonstrate that endogenous levels of atrial peptide are significantly elevated in the plasma of rats with bilateral ureteral obstruction (BUO) compared with control rats or rats with unilateral ureteral obstruction. The contribution of endogenous atrial peptide to the natriuresis and diuresis that follows release of BUO was examined by the intravenous infusion of heparin with or without the exogenous administration of atrial peptide. Infusion of heparin, which binds atrial peptide and interferes with its biological effect, decreased the natriuresis and diuresis observed after release of BUO. Heparin administration also markedly blunted the natriuresis and diuresis observed after exogenous administration of atrial peptide following release of BUO in rats. In contrast, heparin administration did not decrease the natriuresis and diuresis seen in the experimental kidney after relief of unilateral ureteral obstruction. The finding of increased plasma levels of atrial peptide in rats with bilateral ureteral obstruction together with the decrease in diuresis and natriuresis observed with the administration of heparin after release of BUO in these animals indicate that endogenous levels of atrial peptide contribute to the natriuresis and diuresis that occur after release of BUO in rats.

Animals↗

A micropuncture study of proximal tubular transport of lithium during osmotic diuresis.

Lithium and sodium are normally reabsorbed in parallel with water by the renal proximal tubule whereby their tubular fluid-to-plasma concentration ratios (TF/P) remain close to unity throughout the proximal convoluted segment. During osmotic diuresis, the late proximal (TF/P)Na is known to decrease. The present experiments were undertaken to study whether the late proximal TF/P for Li decreases like that of Na during osmotic diuresis. Data were obtained in a control period (C) and in two successive periods during mannitol diuresis (P1, P2). Glomerular filtration rate decreased gradually during osmotic diuresis [1,147 +/- 32 (C) to 950 +/- 22 (P2) microliters.min-1.g kidney wt (KW)-1, P less than 0.01), whereas Li clearance (CLi) increased [377 +/- 21 (C) to 469 +/- 28 (P1, P less than 0.01) and 408 +/- 25 (P2, NS) microliters.min-1.gKW-1, respectively]. (TF/P)Na decreased from 0.98 +/- 0.02 (C) to 0.89 +/- 0.02 (P less than 0.01) and 0.90 +/- 0.04 (P less than 0.05) (P1 and P2, respectively). (TF/P)Li was close to, but significantly higher than, unity during control (1.09 +/- 0.02), but, in contrast to (TF/P)Na, it did not decrease significantly during osmotic diuresis. Delivery of water from the proximal straight segment, as estimated from CLi/CIn, increased in proportion to the delivery from the convoluted segment, as estimated from 1/(TF/P)In. It is concluded that the proximal net Li reabsorption follows more closely the net water reabsorption than the net Na reabsorption during osmotic diuresis.

Absorption↗

Influence of water diuresis on antimicrobial treatment of enterococcal pyelonephritis.

In the present studies, the effect of ampicillin (40 mg intramuscularly twice a day) in combination with water diuresis, produced by the ingestion of 5% dextrose in water, was determined on renal titers of enterococci after intravenous inoculation of 4 x 10(8)-2 x 10(9) enterococci into rats. Ampicillin injections with or without diuresis were started 4 or 21 days after initiation of infection and continued for 7 or 14 days. In comparison to controls (saline injections in rats drinking tap water), diuresis plus saline injections did not lower renal titers of enterococci. Injection of ampicillin in nondiuresing rats had little effect on renal titers of enterococci after 7 days of treatment started 4 or 21 days after initiation of infection. However, 2 wk of ampicillin therapy resulted in a significant decrease in renal titers. The addition of water diuresis to ampicillin treatment markedly potentiated the effect of ampicillin alone in decreasing renal titers of enterococci after 1 or 2 wk of therapy.These studies demonstrate that diuresis resulting from administration of dextrose in water plus ampicillin starting 4 or 21 days after intravenous injection of enterococci reduces renal titers more than ampicillin or diuresis alone.

Ampicillin↗

The pathogenesis of post-obstructive diuresis. The role of circulating natriuretic and diuretic factors, including urea.

To investigate the pathogenesis of post-obstructive diuresis, a state of functional "anuria" during ureteral obstruction was created in awake rats by (a) bilateral obstruction (BO); (b) unilateral obstruction and contralateral nephrectomy (UO-Nx); or (c) unilateral obstruction and continuous i.v. reinfusion of urine from the intact contralateral kidney (UO-reinf). These groups were compared with unilaterally obstructed (UO) and sham-operated control (sham) rats. After release of obstruction of 24 h duration, mean urine flows (V) and sodium excretion rates (UNaV) were significantly elevated above those of sham rats in BO, UO-Nx, and UO-reinf animals, but slightly decreased in UO rats. Glomerular filtration rates were comparably depressed in UO, BO, UO-Nx, and UO-reinf rats. These results suggest that post-obstructive diuresis is due to one or more circulating diuretic factors that are normally excreted in the urine, and which, when retained )as in BO or UO-Nx rats) or returned to the circulation (as in UO-reinf rats), exert a diuretic affect. In additional experiments, UO rats infused with urea exhibited post-obstructive diuresis, if extracellular volume contraction was prevented. This result suggests that urea may be an important diuretic factor in post-obstructive diuresis, but does not exclude possible roles for other humoral factors. The intact kidney of UO-reinf rats displayed a massive unilateral diuresis and natriuresis, further suggesting the presence of potent diuretic factors in the urine. A marked increase in the fractional excretion of glomerular filtrate (V/GFR) by the intact kidney suggests that this diuresis may be attributable, in part, to impaired proximal reabsorption.

Aminohippuric Acids↗

Interactions between nitric oxide and renal nerves on pressure-diuresis and natriuresis.

The present study examined the effect of renal denervation on the impairment of the pressure-diuresis response produced by nitric oxide synthesis blockade. The experiments were performed in Inactin-anesthetized Munich-Wistar rats. The animals with innervated kidneys had lower baseline values of renal blood flow, GFR, sodium excretion (UNaV), and urine flow (V) than rats with denervated kidneys. Also, renal denervation shifted pressure-diuresis and natriuresis toward lower pressures. A low dose of N(omega)-nitro-L-arginine methyl esther (NAME, 3.7 nmol/kg per min) reduced UNaV and the fractional excretion of sodium (FENa) and blunted pressure-natriuresis only in rats with innervated kidneys, whereas it had no effects in rats with denervated kidneys. A medium dose of NAME (37 nmol/kg per min) lowered FENa only in rats with innervated kidneys. The administration of NAME (37 nmol/kg per min) blunted pressure-diuresis and natriuresis in kidneys with or without the renal nerves, but the effect was more pronounced in rats with innervated kidneys. A high dose of NAME (3.7 micromol + 185 nmol/kg per min) increased UNaV and FENa only in rats with innervated kidneys, whereas it reduced GFR, V, UnaV, and FENa in rats with denervated kidneys. However, pressure-natriuresis and diuresis were blunted by this high dose of NAME independently of the presence or absence of renal nerves. These results demonstrate that renal nerves potentiate the renal effects of low doses of NAME on renal function and pressure-diuresis and natriuresis. However, high doses of NAME abolish pressure-diuresis independently of renal nerves, and the natriuretic effect of NAME in innervated kidneys may be attributed to reflex inhibition of sympathetic tone due to the rise in arterial pressure.

Analysis of Variance↗

Renal function correlates of postnatal diuresis in preterm infants.

A characteristic pattern of fluid homeostasis occurs in the first week of life in many preterm infants. Initially, urine output is low independent of fluid intake, subsequently a diuresis occurs, and finally urine output begins to vary with intake. Renal clearance measurements were made during each of these three phases to elucidate the renal mechanisms involved. Periods during which the ratio of urine output to fluid intake was greater than or equal to 1 and urine output was greater than or equal to 3 mL/kg/h were defined as diuretic. Of 22 preterm infants studied from 12 to 120 hours of age, 17 had at least one period of diuresis. In these infants, urine output, fluid intake rate, output to intake ratio, glomerular filtration rate, and fractional sodium excretion were lowest at 12 to 24 hours of age. During diuresis, urine output tripled without a significant change in fluid intake so that output to intake increased to levels exceeding unity. Diuresis was associated with significant increases in glomerular filtration rate and fractional sodium excretion. By 108 to 120 hours of age, urine output decreased despite an increase in fluid intake. This was accompanied by a decrease in glomerular filtration rate. These results suggest that the initial antidiuretic phase is the result of a low fractional sodium excretion in the face of a low glomerular filtration rate. Subsequently, diuresis and natriuresis occur as a result of abrupt, nonmaturational increases in glomerular filtration rate and fractional sodium excretion. With cessation of diuresis, glomerular filtration rate and fractional sodium excretion decrease and water and electrolyte output begin to vary appropriately with intake.

Age Factors↗

Diuresis during fluid infusion : buffer nerve and spinal influences on it.

The rate and cumulative volume of diuresis were measured sequentially for each incremental infusion dose of 5 ml/kg body weight till a 100 ml/kg or more dose was reached. Normal saline (NS), Ringer-Locke (RL) and tender coconut water (TCW) were infused in three groups each of paraldehyde (PLD), and chloralose and urethane (C & U) anaesthetised dogs. The slow infusion rate of about 0.5 ml/kg/min was used. The RL infusion was repeated in vagotomised and/or carotid sinus (CS) denervated dogs and spinal dogs with or without intact vagi. During the NS and RL infusion schedules in PLD anaesthetised dogs produced much less urine than C & U groups. The order of minimum to maximum diuretic effect caused by these fluids were RL, NA and TCW in PLD groups and NA, TCW and RL in C & U groups. The study indicates that the type of anaesthesia and the composition of infusion fluid determines the rate of infusion induced diuresis. PLD anaesthesia has antidiuretic effect, which is not overcome by vagotomy. In C & U anaesthetised dogs the vagotomy and CS denervation performed separately greatly increased the rate of infusion induced diuresis but the diuresis largely decreased when combined surgery was performed. The diuresis in spinal dogs was very low, though in the vagotomised-spinal dogs, the rate of diuresis was more than in the spinal dogs.

Animals↗

Metoclopramide does not inhibit atrial natriuretic factor-stimulated diuresis in man.

BACKGROUND: An understanding of the reflex hormonal responses that occur with a redistribution of the blood volume upon exposure to microgravity or during water immersion is operationally relevant. Further, dopamine receptor antagonists, which are used in the treatment of the motion sickness induced by microgravity, or at sea, may affect fluid metabolism. Atrial natriuretic factor (ANF) is a potent diuretic and natriuretic hormone that is released following central blood volume expansion in man. ANF is also a potent inhibitor of angiotensin- and potassium-stimulated aldosterone release. HYPOTHESIS: Since ANF-induced diuresis may be mediated by dopamine, we sought to determine whether inhibition of dopamine receptors blocks ANF-induced natriuresis and diuresis. Also, since ANF has been shown to inhibit aldosterone secretion induced by adrenocorticotropic hormone (ACTH) in vitro, we investigated whether ANF decreases aldosterone in man infused with exogenous ACTH. METHODS AND RESULTS: In six healthy, sodium-replete men, infusion of synthetic ANF (0.01 microgram.kg.min, Anaritide, Wyeth Laboratories) significantly increased urine flow from 7.1 +/- 0.7 to 11.7 +/- 1.8 ml.min-1 (p < 0.05) and decreased aldosterone from 74.7 +/- 9.0 to 55.8 +/- 6.5 pg.ml-1 (p = N.S.). Metoclopramide (Met), a dopaminergic antagonist, increased plasma aldosterone from 104.5 +/- 8.9 to 163 +/- 12.5 pg.ml-1 (p < 0.05). ANF-induced diuresis was not inhibited by Met, but ANF significantly inhibited Met-stimulated increases in plasma aldosterone. ANF did not attenuate ACTH-stimulated increases in plasma aldosterone. Also, ANF-induced diuresis and natriuresis were not affected by concomitant infusions of ACTH, but the ANF-induced kaliuresis was significantly attenuated by ACTH. CONCLUSION: These studies suggest: a) Synthetic ANF induces a diuresis, natriuresis and kaliuresis; b) the D2 receptor antagonist Met increases plasma aldosterone; c) ANF-induced diuresis is not subject to dopaminergic blockade with Met, but Met-induced increases in plasma aldosterone are inhibited by ANF; and d) ANF does not attenuate ACTH-stimulated increases in mineralocorticoid production. These studies have operational significance, as they demonstrate that D2 dopaminergic blockade by the antinausea agent metoclopramide does not prevent the effects of increased ANF in response to central volume expansion such as occurs during exposure to microgravity or following water immersion.

Adrenocorticotropic Hormone↗